Vasopressin (antidiuretic hormone), a potent vasoconstrictor, is secreted by the posterior pituitary gland in response to hemorrhage (see 41).
The plasma concentration of vasopressin rises progressively as arterial blood pressure diminishes (
Fig. 19.23 ). The receptors responsible for the augmented release of vasopressin are the aortic arch and carotid sinus baroreceptors (high pressure) and stretch receptors in the left atrium (low pressure).
The diminished renal perfusion during hemorrhagic hypotension leads to the secretion of renin from the juxtaglomerular apparatus (see
Chapter 35).
This enzyme acts on a plasma protein, angiotensinogen, to form the decapeptide angiotensin I, which in turn is cleaved to the active octapeptide angiotensin II by angiotensin-converting enzyme; angiotensin II is a very powerful vasoconstrictor.
Renal Conservation of Salt and Water
Fluid and electrolytes are conserved by the kidneys during hemorrhage in response to various stimuli, including increased secretion of vasopressin, as noted previously (see
Fig. 19.23 ), and increased renal sympathetic nerve activity, which enhances NaCl reabsorption by the nephron (decreased excretion). The lower arterial pressure decreases •Fig. 19.22 Changesinarterialbloodpressureandplasmacolloid osmoticpressureinresponsetowithdrawalof45%oftheestimated•Fig. 19.23 Meanpercentagechangesinarterialbloodpressureandbloodvolumeovera30-minuteperiod,beginningattime0.(Redrawnplasmavasopressinconcentrationinresponsetobloodloss.(RedrawnfromZweifachBW.Anesthesiology. 1974;41:157.)fromShenYT,etal.Circ Res. 1991;68:1422.) the glomerular filtration rate, which also curtails the excretion of water and electrolytes. In addition, the elevated levels of angiotensin II, as described earlier, stimulate the release of aldosterone from the adrenal cortex. Aldosterone, in turn, stimulates reabsorption of NaCl by the nephrons. Thus NaCl and water excretion is decreased (see also
Chapter 35).
In contrast to negative feedback mechanisms, hemorrhage also evokes latent positive feedback mechanisms. These mechanisms exaggerate any primary change initiated by the blood loss. Specifically, positive feedback mechanisms aggravate the hypotension induced by blood loss and tend to initiate vicious cycles, which may lead to death.
Whether a positive feedback mechanism will lead to a vicious cycle depends on the gain of that mechanism. Gain is the ratio of the secondary change evoked by a given mechanism to the initiating change itself. A gain greater than 1 induces a vicious cycle; a gain of less than 1 does not. Consider a positive feedback mechanism with a gain of 2. If Pa were to decrease by 10 mm Hg, a positive feedback mechanism with a gain of 2 would then evoke a secondary reduction in pressure of 20 mm Hg, which in turn would cause a further decrease of 40 mm Hg. Thus each change would induce a subsequent one that is twice as great. Hence, Pa would decline at an ever-increasing rate until death occurred. This process is depicted in curve B in
Fig. 19.20
Conversely, a positive feedback mechanism with a gain of 0.5 also exaggerates any change in Pa, but the change would not necessarily lead to death. If arterial pressure suddenly decreased by 10 mm Hg, a positive feedback mechanism would initiate a secondary, additional fall of 5 mm Hg. This decrease, in turn, would provoke a further decrease of 2.5 mm Hg. The process would continue in ever-diminishing steps until arterial pressure approached an equilibrium value.